Leptin is a hormone secreted mainly by fatty tissue. When leptin is secreted into circulating blood, leptin subdues food intake or promotes energy expenditure via leptin receptors in a hypothalamus and a brain stem, thereby reducing body weight.
Recently, there has been reported so-called “leptin resistance” which means decrease in the function of leptin in spite of increase in circulating leptin levels (see Non-patent Literature 1).
There have been conceived many causes as a mechanism behind acquisition of leptin resistance. For example, Non-patent Literatures 2, 6, and 7 describe that protein tyrosine phosphatase 1B contributes to leptin resistance.
Further, Non-patent Literatures 3 and 4 describe that increased expression of suppressor of cytokine signaling 3 (SOCS3) induces leptin resistance. Further, Non-patent Literature 5 suggests that some causes of induction of leptin resistance would be due to a failure of a system which transports circulating leptin to a central nervous system, i.e. blood-brain barrier, rather than reactivity of leptin itself.
Recently, it has been conceived that leptin resistance is a cause for diabetes, hypertension, hyperlipemia, arteriosclerosis etc. Ameliorating and/or preventing leptin resistance is important also for ameliorating and/or preventing diseases resulting from leptin resistance.
For example, Patent Literature 1 discloses a pharmaceutical composition for ameliorating endoplasmic reticulum stress in central nerve. Such a pharmaceutical composition is characterized by containing a nonsteroidal anti-inflammatory compound. Patent Literature 1 suggests that flurbiprofen is usable as the nonsteroidal anti-inflammatory compound.